Meerson F Z
Clin Cardiol. 1983 Apr;6(4):163-70. doi: 10.1002/clc.4960060403.
Recently, it has been shown that nonischemic parts of the heart in myocardial infarction were separated from ischemic damaged ones by a sharp border zone. In this connection, the disturbance of contractile function of the myocardium of nonischemic parts is suggested to result from the infarction-concomitant emotional-painful stress. In order to test this assumption, the contractile function of the right auricle, which is an a priori nonischemic heart division, was studied in rats subjected to myocardial infarction of the left ventricle. In the study of the isolated auricle the following facts were established: 1 day after the induced infarction the atrial myocardium shows reduced extensibility, depression of the Starling curve, a concomitant approximately twofold decrease of the maximal systolic tension, and a reduced myocardial resistance to hypoxia and calcium excess. This complex of shifts, first, is completely reproduced without myocardial infarction by emotional-painful stress and, second, can be prevented to a considerable extent by propranolol indicating that it is essentially stress induced. In infarction, these above said stress-induced disturbances of the contractile function of nonischemic divisions of the heart were found to be prevented or limited by factors stabilizing the membranous lipid bilayer of cardiomyocytes, i.e., by antioxidant ionol, by nicotinamide, a lipase inhibitor, and by chloroquine, a phospholipase inhibitor. The aspects of application of these factors for the therapy of ischemic heart disease requires further studies.
最近研究表明，心肌梗死中心脏的非缺血部分与缺血损伤部分之间由一个明显的边界区分开。就此而言，非缺血部分心肌收缩功能的紊乱被认为是由梗死伴随的情感性疼痛应激所致。为了验证这一假设，对左心室发生心肌梗死的大鼠的右心耳（其本身是一个非缺血性心脏分区）的收缩功能进行了研究。在对分离的心耳的研究中确定了以下事实：诱导梗死1天后，心房肌的伸展性降低，斯塔林曲线下降，最大收缩张力随之降低约两倍，心肌对缺氧和钙过量的耐受性降低。首先，这种变化组合在没有心肌梗死的情况下通过情感性疼痛应激完全再现；其次，普萘洛尔可在很大程度上预防这种变化组合，这表明它本质上是由应激诱导的。在梗死中，发现上述由应激诱导的心脏非缺血分区收缩功能紊乱可被稳定心肌细胞膜脂质双层的因素所预防或限制，即抗氧化剂维生素E、脂肪酶抑制剂烟酰胺和磷脂酶抑制剂氯喹。这些因素在缺血性心脏病治疗中的应用方面需要进一步研究。
